Markedly elevated specific renin levels in the adrenal in genetically hypertensive rats.

Naruse, Mitsuhide; Inagami, Tadashi

doi:10.1073/pnas.79.10.3295

Cited by 78 publications

(37 citation statements)

References 48 publications

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“…Previously Naruse and Inagami 6 showed that adrenal renin continued to increase after bilateral nephrectomy when plasma active renin was very low; we confirmed these results and demonstrated that the increase in renin was confined to the zona glomerulosa cells.…”

Section: -13supporting

confidence: 78%

Role of the adrenal renin-angiotensin system on adrenocorticotropic hormone- and potassium-stimulated aldosterone production by rat adrenal glomerulosa cells in monolayer culture.

et al. 1990

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The rat zona glomerulosa has a renin-angiotensin system that appears to function as an autocrine or paracrine system in the regulation of aldosterone production. To further investigate dynamic changes of production of renin and aldosterone in vitro we developed a primary monolayer culture of rat adrenal glomerulosa cells in serum-free medium. Collagenase-dispersed glomerulosa cells were incubated in PFMR-4 medium containing 10% fetal calf serum for 48 hours; the medium was then replaced with serum-free PFMR-4 medium. The cell viability and the aldosterone secretion were stable over the additional 48 hours in the serum-free control medium. After incubation for 24 hours in the serum-free medium, the cells were exposed to high K + or adrenocorticotropic hormone (ACTH) for another 24 hours. ACTH stimulated aldosterone secretion, and this increased secretion was associated with an increase in renin activity ( demonstrated. These observations provide evidence that the renin found in the adrenal is, at least in part, synthesized locally. Our laboratory also has shown that adrenal renin increases after a low sodium or high potassium diet and after nephrectomy and that there is a positive correlation between adrenal renin and adrenal aldosterone concentration. -11 Recently, we showed that almost all of renin mRNA was in the adrenal zona glomerulosa with very little in the zona fasciculatareticularis and that the renin mRNA increased after sodium depletion in the rat. 17 These observations suggest that adrenal renin synthesized in glomerulosa cells may be a possible regulator of aldosterone secretion.Recently, our laboratory investigated the production of renin, angiotensin II, and aldosterone in rat adrenal capsular explant cultures in serum-free me-

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Section: -13supporting

confidence: 78%

Role of the adrenal renin-angiotensin system on adrenocorticotropic hormone- and potassium-stimulated aldosterone production by rat adrenal glomerulosa cells in monolayer culture.

et al. 1990

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“…Secretion of renin by the kidney increases in these conditions and renin in plasma may act upon its substrate to generate AI. However, renin is present in many organs (3)(4)(5)(6) and cell types (7)(8)(9), including vascular smooth muscle cells (8); AI and All and converting enzyme exist in renin-containing cells (7,9,10); and the plasma concentration of All is in the picomolar range (1 1), but binding affinities of this peptide to its receptors are in the nanomolar range (12)(13)(14)(15). These observations raise questions about the role of circulating renin and angiotensin.…”

Section: Introductionmentioning

confidence: 99%

Local generation of angiotensin II as a mechanism of regulation of peripheral vascular tone in the rat.

Oliver¹,

Sciacca²

1984

J. Clin. Invest.

115

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Abstract. Renin is present in vascular smooth muscle cells and has been shown to coexist with angiotensins I (Al) and II (All) in many cell types. Accordingly, we postulated that the renin-angiotensin system controls vascular tone, not by the action of circulating renal renin but rather, by the local generation of angiotensin by vascular renin. Isolated rat hindquarters were perfused in vitro with Krebs-Henseleit buffer containing 7% albumin, and flow-adjusted to obtain a perfusion pressure of -90 mmHg. Infusion of 4.8 nmol* min-' for 5 min of All or Al markedly increased perfusion pressure. An identical dose of the synthetic tetradecaptide of renin substrate (TDCP-RS) increased pressure similarly to Al. The pressure increase evoked by TDCP-RS was markedly decreased by captopril and by two different peptides that inhibit renin. Renin activity in the perfusate, incubated with semipurified rat renin substrate, was 21±3 pg Al ml-' h-' (mean±SEM) at 15 min of perfusion and 47±4 pg Al -ml-' -h-' at 45 min (n = 9; P < 0.01). When TDCP-RS was infused at 4.8 nmol * min-' for 5 min in the presence of captopril, Al in the perfusate increased linearly at a rate of 16.5 pmol min-' for 10 min (n = 5). The results indicate that TDCP-RS constricted the vasculature by its conversion to All and suggest that All was generated from a two-step hydrolysis of TDCP-RS by renin and converting enzyme. The data thus suggest that the renin-angiotensin system controls vascular tone by the local generation of All by renin and converting enzyme in the vasculature.

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“…29 Although the exact physiological function of intra-adrenal renin is unclear, local generation of Ang I and II may play a modulatory role in aldosterone secretion by affecting activity of biosynthetic enzymes or angiotensin receptors. In view of the reduced Ang II receptors we found in SHR, it is of interest that Naruse and Inagami 30 have reported markedly increased adrenal renin content in SHR. Although we did not measure adrenal renin content in our studies, it seems quite possible that the abnormal regulation of receptors we observed could be related to abnormalities in local, intra-adrenal, or periadrenal Ang II generation.…”

Section: Adrenal Ang II Receptor Regulationmentioning

confidence: 90%

Abnormal regulation of adrenal angiotensin II receptors in spontaneously hypertensive rats.

Bradshaw

Moore

1988

Hypertension

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SUMMARYThe aldosterone response to angiotensin II is blunted in spontaneously hypertensive rats (SHR). To determine whether this blunting is due to a defect in angiotensin II receptors, we assessed angiotensin II binding to intact adrenal glomerulosa cells in SHR and normotensive WistarKyoto rats (WKY) that had been fed high or low sodium diets before sacrifice. In rats on high salt intake, we observed no difference between the two strains in either receptor affinity (K d = 1.0-1.2 nM) or binding capacity (36,000-38,000 receptors/cell). When sodium-restricted, WKY increased receptor content more than fourfold to 167,000 sites/cell. SHR increased receptor number to only 103,000 sites/cell, which was significantly (p<0.01) less than the WKY increase. The cause of the abnormal receptor regulation remains unclear. Two known receptor regulators, the plasma angiotensin II level and the state of potassium balance, were similar in the two strains. Our results suggest that the blunted aldosterone response to angiotensin previously reported in SHR is due to abnormal angiotensin receptor up-regulation in the adrenal gland in response to sodium restriction.

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Markedly elevated specific renin levels in the adrenal in genetically hypertensive rats.

Cited by 78 publications

References 48 publications

Role of the adrenal renin-angiotensin system on adrenocorticotropic hormone- and potassium-stimulated aldosterone production by rat adrenal glomerulosa cells in monolayer culture.

Role of the adrenal renin-angiotensin system on adrenocorticotropic hormone- and potassium-stimulated aldosterone production by rat adrenal glomerulosa cells in monolayer culture.

Local generation of angiotensin II as a mechanism of regulation of peripheral vascular tone in the rat.

Abnormal regulation of adrenal angiotensin II receptors in spontaneously hypertensive rats.

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